During an infection, invading microbes can be caught in sticky webs of chromatin (DNA + histones) that are released by neutrophils. These neutrophil extracellular traps are decorated with granules that are laden with lytic enzymes and antimicrobial peptides; these weapons facilitate the rapid killing of pathogens.

In small-vessel vasculitis (SVV), the body generates antibodies against two antigenic proteins that are expressed by neutrophils, and this leads to the inflammation of small blood vessels. How this chronic condition is sustained has not been clear, but Kessenbrock et al. have found that these nets are also produced in the absence of infection and that they may perpetuate autoimmune disorders. It appears that when neutrophils are attacked by these autoantibodies, they release their fibrous chromatin nets (shown above), which contain the two antigens. Kidney biopsies from patients with SVV confirmed the presence of neutrophils and nets near deteriorating capillaries. This immune response probably maintains the exposure of the autoantigens to other immune cells (dendritic and B cells), whose consequent activation could play a pathogenic role in the disease.